1. Field of the Invention
The present invention generally relates to determination and monitoring of vital signs and more particularly relates to accurate determination and monitoring of vital signs by detecting contraction and expansion in the vascular bed of the lining tissue of the external auditory canal.
2. Description of the Related Art
As described in the U.S. Pat. No. 6,454,718, issued to the applicant, the signal present at the external auditory meatus and canal, “the external auditory canal”, is a combination of blood pressure and respiratory signals. The respiratory signal itself is produced by simultaneous pressure events in the structures of the head and neck. These include the transmission of pressure changes in the naso-pharynx and trachea, the expansion and contraction of intrathoracic blood vessels and cardiac volume and changes in muscle tone in the accessory muscles of respiration.
The process of breathing is a complex process involving, “ventilation” or movement of gases, “diffusion” or transport of gases across the alveolar epithelium and perfusion movement of blood into and out of the lung. Pathology effecting one or all of these areas can and does occur with the net effect being short of breath. However, different therapeutic interventions require a clear understanding of the relative decrease in each of these areas and this require different diagnostic sensors or approaches to be used simultaneously.
In fact, application of any therapy without understanding what is going on with each area can be detrimental if not fatal. Even the application of oxygen can lead to fatal consequences through the suppression of hypoxic drive and CO2 retention, if the pathology is not understood.
In true physics terms, air is not sucked into the lungs, but is pushed in by the atmospheric pressure when the relative intra thoracic pressure is lowered below the point where it overcomes airways resistance. In mechanical terms, the muscles supporting the rib cage and the diaphragm itself contract in such a way as to increase the volume of the rigid chest wall. The accessory muscles lift and separate the ribs like a bellows and the diaphragm pulls down toward the abdomen. The pliable, sponge-like lung tissue expands to fill the vacuum produced and air is drawn into the lungs through airways.
Understanding this mechanism helps to explain the various pathologies that affect a patient who is having trouble breathing. At the outside, failure of the muscles to contract as a result of fatigue or neurological injury prevents the expansion of the chest cavity. Several conditions can be lead to paralysis of the diaphragm and the flail muscle moves passively in and out as the patient breathes. Only if the accessory muscles of respiration, such as the intercostals, trapezius and pectorals can expand the chest cavity to overcome the loss of the diaphragm contribution will the patient be able to survive.
Expansion of an intra-abdominal contents, such as with gastric outflow obstruction, mechanically restricts movement of the chest wall and pushes the diaphragm high into the chest cavity. At extremes, this prevents generation of the negative intrathoracic pressure and the patient suffocates.
A multiple rib fracture produces a flail segment of chest wall which can move in and out with respiration, though usually tethered by muscle and tendon, if the ribs are broken in enough places there is no rigid structure to produce the vacuum against and the patient must receive positive pressure ventilation to survive.
If the lung itself is less compliant such as with pneumonia or cardiac failure then the work of expanding the lung is increased. In addition, if the airways are narrowed such as with asthma, the pressure required to produce the same degree of air movement is markedly greater.